Acid-base regulation in prolonged hypoxia: Effect of increased P CO 2

Abstract

Conscious rats maintained for 3 wk at PB 370–380 Torr were studied in a chamber where PI O 2 was kept at 68–70 Torr at ambient barometric pressure (740–750 Torr). Blood samples were obtained through an arterial catherer. Controls were pair-fed rats maintained at ambient barometric pressure and studied at PI O 2 68–70 Torr for 4 h (acute hypoxia) or at ambient PI O 2 (normoxia). Arterial blood pH of 3-wk hypoxic rats was not different from that of normoxic rats. Hypercapnia was produced by increasing PI CO 2 for 4 h. The 3-wk hypoxic rats showed the highest apparent non-bicarbonate buffer value of arterial blood ( βapp): 77 mmol/(pH·kg), compared to 38 in normoxia and 43 mmol/(pH·kg) in acute hypoxia. Comparison of βapp at different times of hypercapnia in intact and in nephrectomized rats suggests that the high βapp of prolonged hypoxia is largely due to an increased renal compensation, and, to a smaller extent, to increased chemical buffering. While the extracellular fluid of normoxic and acute hypoxic rats showed a net gain of base of non-renal origin during hypercapnia, the 3-wk hypoxic rats showed a net non-renal base loss, which may be ,asked by the increased renal compensation.